Transposons are mobile DNA elements that constitute a large fraction of most eukaryotic genomes. These parasitic genetic elements propagate by multiplying within the genomes of host germ cells. While the majority of transposable element copies are nonfunctional, a subset have retained the ability to mobilize when host control mechanisms are compromised. Because of their potential to copy themselves and insert into new genomic locations, as well as to generate enormous levels of expression, transposable elements present a massive endogenous reservoir of genomic instability and cellular toxicity. Although most investigations have naturally focused on the germline, where new insertions are heritable and thus favored by transposon evolution, somatic tissues also have an active transposon silencing mechanism whose functional significance is less understood. Understanding transposon control mechanisms requires novel genomic techniques, for example to assess transcriptional versus !
post-transcriptional pathways, which are both known to contribute to transposon control in animal cells. Analyzing these datasets requires dedicated bioinformatic algorithms to handle the complexities of mapping and accounting for short reads from highly repetitive regions of the genome. This talk will focus on the complexities of genomic analysis in the transposon realm through two related studies. The first story will focus on using the drosophila ovary to understand the differences between germline and somatic transposon control mechanisms. The second part of the talk will focus on the possible consequences of unleashing transposons in the human brain: a particular example of the importance of transposon control in somatic tissues.